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Polymorphisms in tumour necrosis factor (TNF) are associated with risk of bladder cancer and grade of tumour at presentation.

ABSTRACT: The purpose of this study is to assess the role of tumour necrosis factor (TNF) polymorphisms in the risk of developing bladder cancer and effect on tumour stage, grade and progression. In all, seven single-nucleotide polymorphisms in TNF were studied in 196 bladder cancer patients and 208 controls using a PCR-SSP genotyping technique. It was seen that there was a significant association of two polymorphisms in TNF with bladder cancer: the TNF+488A allele was found in 28.1% of patients compared with 14.9% of controls (P=0.0012). In addition, TNF-859T was found in 26.0% of patients compared with 14.4% of the controls (P=0.0036). The two loci were in tight linkage disequilibrium, that is, almost all the individuals having TNF+488A also had TNF-859T. Patients with the TNF+488A or TNF-859T were more likely to present with a moderately differentiated tumour than those patients without the uncommon allele. In all, 16.7% of patients with TNF+488A and 29.9% of patients without TNF+488A presented with a G1 tumour (P=0.015). A total of 14% of patients with TNF-859T and 30.5% of patients without TNF-859T presented with a G1 tumour (P=0.0043). There was no significant effect on time to first recurrence, stage progression or grade progression. In conclusion, a significant association between TNF polymorphisms TNF+488A and TNF-859T and risk of bladder cancer was detected in this study. Both these polymorphisms were associated with grade of tumour at presentation although there was no significant effect on subsequent tumour behaviour.

SUBMITTER: Marsh HP

PROVIDER: S-EPMC2376948 | biostudies-other | 2003 Sep

REPOSITORIES: biostudies-other

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Project description:Inflammation is one of the early phases in the development of gastric cancer. Therefore, several studies have examined the association of polymorphisms in tumour-necrosis factor-A gene (TNF-A) with gastric cancer risk. This meta-analysis reviews and summarises published evidence for these associations. Searching several databases yielded 24 independent studies that reported on the associations between TNF-A polymorphisms and gastric cancer risk. We analysed available data for the most commonly investigated polymorphisms: TNF-A -308G>A (23 studies), TNF-A -238G>A (9 studies), and TNF-A -857C>T (5 studies). Summary odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated in the random-effects model using the DerSimonian-Laird method. Q-statistic and I(2)-statistic were calculated to examine heterogeneity, and funnel plots were plotted to examine small study effects. The overall ORs (95% CIs) for AG and AA genotypes vs GG genotype for TNF-A -308 were 1.09 (0.94-1.27) and 1.49 (1.11-1.99), respectively. For TNF-A -238, the corresponding ORs (95% CIs) were 1.05 (0.84-1.33) and 1.25 (0.30-5.26), respectively. The overall ORs (95% CIs) for CT and TT genotypes (vs CC) for TNF-A -857 were 1.06 (0.89-1.27) and 1.57 (0.91-2.70), respectively. The statistically significant association between TNF-A -308GG and gastric cancer was limited to western populations. This association showed little heterogeneity (I(2)=0) and remained consistently strong when analyses were limited to anatomic and histologic subtypes of gastric cancer, or limited to studies in which genotype frequencies were in Hardy-Weinberg equilibrium, or limited to larger studies. These same subgroup analyses did not change results associated with other polymorphisms. In conclusion, TNF-A -308AA genotype was associated with a statistically significant increased risk of gastric cancer, whereas other studied polymorphisms were not. The association between TNF-A -857TT genotype and gastric cancer was near significant, and may become significant if more studies are published.

Project description:Individual studies have assessed the association between TNF-α-308G>A and TNF-α-238 G>A polymorphisms and severity of dengue infection. However, the results are inconclusive and most studies had small sample sizes. The objective of this study was to summarize the evidence of association between TNF-α-308 G>A and TNF-α-238 G>A and severity of dengue infection. This study follows the preferred reporting items for systematic reviews and meta- analyses of genetic association studies, recommended by PLOS One. We calculated pooled odds ratio and its 95% confidence interval (CI) to estimate the association between TNF-α-308 G>A or TNF-α-238 G>A and the risk of severe dengue infections. To determine the information size required for this meta-analysis study, a trial sequential analysis (TSA) was done. Eight studies (640 cases and 1275 controls), which assessed the association of TNF-α-308 G>A or TNF-α-238 G>A and the risk of DHF were included. Overall, we found no significant association between TNF-α-308 G>A and the DHF risk in the allelic model (OR, 0.91; 95% CI, 0.51-1.63), the recessive model (OR,1.32;95%CI,0.73-2.37), the dominant model (OR,0.93;95%CI:0.59-1.47) or the additive model (OR,1.43,95;95%CI:0.79-2.59). There was also no significant association between TNF-α-238 G>A and DHF risk under the allele contrast model (OR:1.51;95%CI:0.88-2.58), the recessive model (OR,1.48,95% CI:0.33-6.58), the dominant model (OR,1.48;95%CI:0.56-3.92), or the additive model (OR:1.5;95%CI:0.34-6.69). On subgroup analysis, neither the Asian population nor the non-Asian population showed significant association between TNF-α-308 G>A/TNF-α-238 G>A and the DHF risk under any genetic models. Leave-one-out meta-analysis showed stability of the results. TSA plots suggested that the sample size in this meta-analysis study was below the required information size. The findings suggest an inclusive evidence of the association between TNF-α-308/ TNF-α-238 G>A and the risk of developing severe dengue infection. Large studies with evidence of Hardy-Weinberg equilibrium, assessing gene-gene interactions are recommended.

Project description:Background:Multiple studies have been carried out examining the association of tumor necrosis factor-? gene (TNF-?) promoter region polymorphisms with recurrent pregnancy loss (RPL) risk. However, the results remain controversial and incomplete. Hence, we performed a meta-analysis to evaluate the association of the TNF-? -308G>A and -238G>A polymorphisms with RPL risk. Materials and Methods:In this meta-analysis, a comprehensive search of PubMed, Web of Knowledge and EMBASE was performed to identify relevant studies published until December 1, 2017. The associations were assessed by odds ratio (OR) and its corresponding 95% confidence interval (CI). Results:A total of 29 case-control studies, comprising 20 studies on TNF-? -308G>A (3,461 cases and 3,895 controls) and nine studies on TNF-? -238G>A (2,589 cases and 2,664 controls), were included in the meta-analysis. Overall, we found TNF-? -308G>A to be associated with an increase in RPL risk under the homozygote (OR=1.716, 95% CI: 1.210-2.433, P=0.002) and the recessive (OR=1.554, 95% CI: 1.100-2.196, P=0.012) models. TNF-? -238G>A was also significantly associated with increased risk of RPL under the allele model (OR=1.554, 95% CI: 1.100-2.196, P=0.012). Stratified analysis revealed a more significant association between theTNF-? -308G>A polymorphism and increased RPL risk in Asians under the homozygote (OR=2.190, 95% CI: 1.465-3.274, P?0.001), the dominant (OR=1.642, 95% CI: 1.269-2.125, P?0.001) and the recessive (OR=1.456, 95% CI: 1.039-2.040, P=0.029) models, but not in Caucasians. A non-significant association was, however, identified between TNF-? -238G>A and RPL risk based on ethnicity. Moreover, TNF-? -308G>A and -238G>A polymorphisms were significantly associated with increased risk of RPL in high quality studies and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) subgroups. Conclusion:The present meta-analysis demonstrates that TNF-? -308G>A and -238G>A polymorphisms are associated with an increased risk of RPL.

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Polymorphisms in tumour necrosis factor (TNF) are associated with risk of bladder cancer and grade of tumour at presentation.

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